Another unintelligent move

Over at the Discovery Institute’s Media Complaints Division, Casey Luskin is keeping himself busy trying to fudge assert that the notion of “junk DNA” (which ID advocates consider erroneous, despite the fact that strong, independent lines of evidence indicate that a large fraction of genomic DNA in most eukaryotic organisms is phenotypically non-functional) was the result of application of Darwinian principles.

Several people (e.g. T. Ryan Gregory, Larry Moran and Steve Reuland, as well as myself ) have already pointed out that, on the contrary, a strict application of the Darwinian paradigm, also known as “panselectionism” or “adaptationism”, led many prominent evolutionary biologists to initially resist the idea that some DNA may be non-functional, an opposition which was later mostly lifted (sometimes partially, as we will see) by the progressive acceptance of neutralist views.

Indeed, as late as 2001 Ernst Mayr, one of the “deacons” of Darwinian adaptationism, thought it appropriate to state, in “What Evolution Is”:

A remarkably high proportion of DNA in the chromosomes seems to perform no obvious function, such as coding for RNAs and proteins. Such DNA, probably incorrectly referred to as “junk,” is estimated for humans to be as much as as 97 percent of the total DNA. […] There is widespread belief among Darwinians that such apparently unnecessary DNA wouldhave been eliminated long ago by natural selection if it did not have some, as of yet undiscovered, function.

(E. Mayr, 2001, What Evolution Is, Basic Books, p. 108)

[Note that for Mayr, never much the pluralist, true DarwiniansTM essentially included only strict followers of the Neo-Darwinian New Synthesis, with minor - ahem - adaptations.]

In “The Growth of Biological Thought” (1982), Mayr also rejected the idea that “junk DNA” may be largely composed of parasitic, “selfish” elements, which, while not strictly non-functional, only serve the goal of their own propagation. Such an idea, Mayr wrote:

is inherently distasteful to a Darwinian. Surely natural selection, a Darwinian would say, should be able to come up with a defense mechanism against such an expensive type of parasitism.(E. Mayr, 1982, The Growth of Biological Thought, Belknap Press, p 579; quoted by Maxine Singer in From Genomic Junk to Human Disease, Proc. Am. Phil. Soc. 138, 11-24, 1994)

In 1971, shortly after the seminal papers by Kimura, King and Jukes and others had formalized and begun to test the Neutral Theory, Mayr threw the gauntlet with words that would fit perfectly in the mouth of most of today’s ID advocates:

More and more sites even in the largest molecules are found to have specific functions. A “functionless site” is simply one the function of which has not yet been determined.

So much for the claim that “junk DNA” was a direct consequence of Darwinian ideas.

But there is a far sweeter contradiction at play here.

On the one side, ID advocates certainly like to claim that the functionality of “junk DNA” is a direct and necessary consequence of the design approach. For instance, in a paper in the now defunct “peer-reviewed” ID journal PCID, Jonathan Wells says:

From an ID perspective, however, it is extremely unlikely that an organism would expend its resources on preserving and transmitting so much “junk.” It is much more likely that noncoding regions have functions that we simply haven’t discovered yet.

while on the other, they have expended significant amounts of effort countering what they claim is the fallacy of the “argument from optimal design”, which points out that biological “design” is at times clearly haphazard and inefficient, reflecting more the contingencies of an undirected evolutionary process than any foresight or intelligent planning. Thus, Bill Dembski wrote, in an article entirely devoted to this topic:

Nevertheless, taken strictly as a scientific theory, intelligent design refuses to speculate about the nature of this designing intelligence. Whereas optimal design demands a perfectionistic, anal-retentive designer who has to get everything just right, intelligent design fits our ordinary experience of design, which is always conditioned by the needs of a situation and therefore always falls short of some idealized global optimum.

[Incidentally, note that this article, written for a religious audience, is not shy at all about using the G-word, and while claiming that ID “refuses to speculate about the nature of this designing intelligence”, it eventually goes off the deep Biblical end:

This is a fallen world. The good that God initially intended is no longer fully in evidence. Much has been perverted. Dysteleology, the perversion of design in nature, is a reality. It is evident all around us. But how do we explain it? The scientific naturalist explains dysteleology by claiming that the design in nature is only apparent, that it arose through mutation and natural selection (or some other natural mechanism), and that imperfection, cruelty, and waste are fully to be expected from such mechanisms. But such mechanisms cannot explain the complex, information-rich structures in nature that signal actual and not merely apparent design–that is, intelligent design.

The design in nature is actual. More often than we would like, that design has gotten perverted. But the perversion of design–dysteleology–is not explained by denying design, but by accepting it and meeting the problem of evil head on. The problem of evil is a theological problem. To force a resolution of the problem by reducing all design to apparent design is an evasion. It avoids both the scientific challenge posed by specified complexity, and it avoids the hard work of faith, whose job is to discern God’s hand in creation despite the occlusions of evil.[8]

Dead code is code that was written into the program in high level programming language, either erroneously, or originally, for some now redundant purpose (such as testing other code), and remains in the program source code doing nothing. Modern compilers, programs that convert source code into computer-interpretable code, usually strip out
such unused code during the process of compilation, analogous to the way in which DNA polymerase excises introns (non-coding sequences) out of a gene and splices together its exons (coding sequences) when transcribing to mRNA. However, the dead code can happily sit in the source code (as perhaps can the ‘junk’ DNA stay in the DNA) forever - doing nothing but causing confusion to later intelligent observers - engineers who must update the program for example.

Sometimes software engineers will leave code that is not dead code, but does not perform a function, in the source code intentionally. Such code is sometimes called a stub, and is incorporated for the purposes of extensibility - extending the capabilities of the code later on. The code is correct and required effort to produce, was deemed unnecessary to the current version of the software, but is desirable to add functions to the next version, and therefore is purposefully left in - by design. Of course, depending on a number of factors - whether requirements for the next version of the software change or other software makes it obsolete before the next version - even code for extensibility might never be used. There are many other examples of code, that might never actually be used, being purposefully incorporated into software programs. Take interface code for example. Software engineers might build software A to talk to or interoperate with software B written by other software engineers. The source code that facilitates this interoperability is called interface code. However, if the software B project is cancelled, then the interface to B from A will likely never be used, but might never be removed. This is just another example of designed flaws or non-optimal design by intelligent designers.

It is also noteworthy that in computer science and engineering, what is actually considered optimal is contingent on many factors relating to the requirements for the design (what people need or want it to do) and how powerfully the design must implement functions to cater for those requirements. For example, the speed of a software module that runs a screensaver is likely to be considered optimal at a much lower bit-rate than one that renders visual radar feedback on the space shuttle.

Ultimately, of course, software engineers are imperfect designers with limited capabilities operating in imperfect conditions (budget, fatigue and delivery schedules etc.), and so no rational person expects their designs to be perfect, flawless, or even necessarily optimal (although they may converge on some of these some of the time). However, even a putatively perfect or superhuman intelligent designer - one capable of designing the biochemical underpinnings of life - is arguably not required to produce perfect, flawless or optimal designs.

So, Intelligent Design predicts efficient design and no “junk DNA”, except when of course it doesn’t. Ah, the power of having a heuristically empty theory!

Ultimately, I think ID’s current infatuation with the “no junk DNA” mantra, jumping on the bandwagon of some recent discoveries, is an altogether bad move for them, for several reasons:
- First, it puts them in the uncomfortable position of aligning themselves with ultra-Darwinian pan-selectionists, who not only have clear dibs on who first expressed skepticism at the existence of “junk DNA”, but also can explain why all DNA should be functional based on a much more elegant and parsimonious theory (based on straightforward, “micro-evolutionary” negative selection effects that even the most close-minded ID advocates would find hard to argue against).
- Second, it forces them into a contradiction with respect to the “argument from optimal design”: either design is optimized, in which case neither “junk DNA” nor our prostates and inverted retinas should exist, or it isn’t.
- Finally, and most importantly, it still leaves them facing the daunting task of explaining away the currently overwhelming evidence (from the c-value paradox, to the existence of large deletion polymorphisms, to the phylogenetic evidence for neutral “drift” of most stretches of intergenic sequence, etc) that much of genomic DNA in many eukaryotes has no phenotypic effect.

Of course, I don’t expect ID advocates to change course at this point, as their penchant for painting themselves into corners (see Behe’s testimony at the Dover trial for a masterpiece in the art) is now the stuff of legend. Still, it will be fun to see how they will cope when reality catches up with them.

[UPDATE:
Casey Luskin has posted another piece at the Discovery Institute’s Media Complaints Division ominously entitled: “Is Panda’s Thumb Suppressing the Truth about Junk DNA?”, in which he alleges that I have suppressed a comment from one Andras J. Pellionisz, who seems to be a rather cranky biophysicist (“of Information Geometry of Nature”, according to his own self-description) who claims to have identified the function of “junk DNA” based on its “fractal geometrical” properties.

The real irony is that Luskin complains of a non-existing instance of censorship here while writing on a site that does not allow any comments whatsoever, and has systematically rejected track-backs from the Panda’s Thumb for years (I am sending one from this post, let’s see if it goes through).

Of course, the “Evolution News & Views” site has no interest in having its readers fairly and publicly evaluate its arguments, like we do at PT. Its goal is simply to administer the Discovery Institute’s Kool-Aid, without interference from uncomfortable questions or pesky facts. ]

[UPDATE II:
Luskin has added the following addendum to his original piece:

Update 8:00 am, July 23, 2007: Unsurprisingly, Dr. Pellionisz now reports that after my post went live, he discovered that Panda’s Thumb chose to post his comment.

Since the comment in question was in fact authorized for publication long before Luskin’s post went live with Pellionisz’s erroneous accusation, either Luskin or Pellionisz (or both) are still blatantly misrepresenting the truth. I’ll let them sort out between themselves who is in fact responsible for the falsehood; in the meanwhile, bets are open.]

Sure, ID predicts the presence of lots of junk DNA. If you go in any house you will almost certainly see some pictures hanging on the wall, or flowers in a vase, or hand-woven baskets on top of the kitchen cabinets. The Interior Designer has included non-functional elements in her design. Non-functionality is a direct and necessary consequence of Interior Design. We can extrapolate, knowing what we do about Interior Designers, how Go–er–the Intelligent Designer designs. On the other hand, if you visit a house furnished by the Bauwowhaus school of Interior Design, functionality rules. The conclusion is that you are absolutely correct when you say

Intelligent Design predicts efficient design and no “junk DNA”, except when of course it doesn’t.

Of course, what are the alternatives? I mean, if they had some good arguments, I’d ask why they don’t focus on those instead of fighting to assert predictions from evolution that never existed, and their insistence that patently worthless junk must have function (it’s probably possible that nearly all has function (if in some redundant capacity, perhaps), but no reasonable scientist would supposes that it did at the present time).

What are they supposed to do, bring up their research triumphs, genuine predictions of ID that have succeeded (well, in fact they failed spectacularly), and their great understanding of malaria evolution? Are they going to tell us how “design” differs from what is expected from evolution, or why the patterns of “design” in prokaryotes differs from the patterns of “design” in eukaryotes (but not from what would generally be predicted from evolution under known constraints)?

They might as well stick with their earlier claims until these no longer sell to the gullible. Then, because they’re fulfilling a need to deny evolution rather than any imperative to deal with models and evidence, they can just find another argument that has no legs scientifically, but can be foisted onto their naive constituents.

On September 1, 2005 when I originated the International PostGenetics Society http://www.postgenetics.org and established PostGenetics (“Genomics beyond Genes”) we reached the “eye of the JunkDNA cyclone”; with an organization standing up against casting out 98.7% of human Genome as “Junk” the overwhelming wind was no longer blowing individual scientists into a junky direction. There appeared an organization, led by scientists, to provide anchorage of research of what this 98.7% actually does. On the 12 of October 2006, on the “European Inaugural” of IPGS there appeared the first international organization that formally abandoned the “JunkDNA” misnomer as a scientific term.

On the 14 of June, 2007, with the publication of the NIH-led ENCODE-report(with $53 M tax-dollars spent), we have reached the dead center of the eye of the cyclone. Yes, as appeared in The Scientist Gallagher Editorial “http://www.the-scientist.com/2007/7/1/15/1/”, in July, the discredited misnomer will liver forever as a memento of “framing” Modern Genetics into an establishment where resources were denied, papers were rejected (ask e.g. Mattick and Taft of their excellent manuscript which was never accepted as intended, or even Rigoutsos whose breakthrough publication on pyknons sustained at least a year of delay). Worse, as I pointed out in my “comments” to The Scientist, elaborated in more detail in an Obituary of Junk DNA “ http://www.junkdna.com/#obituary_of_junk_dna “ uncounted millions of people died of miserable deaths while scientists were looking for the “gene” causing their illnesses - and were not even supposed to look anywhere but under the lamp illuminating only 1.3% of the genome (the genes).

As documented in the full transcript of the video Genius of Junk “http://www.abc.net.au/catalyst/stor[…]/s898887.htm” award-winning science documentary (never aired in the USA, guess why), Malcolm, as a Darwinist voiced in the 2003 filming his 1987 conviction against the “Junk Frame” this way:

“Under Darwinistic notions you would think that junk would drop off under the theory of natural selection just like species drop off if they hit ecological niches which is incompatible with survival. If they can adapt to those niches, then those that can survive and those that can’t die. There’s the notion. If you apply that to the DNA sequence, then the coding region genes which survived have a function and by the way the non coding sequences have survived as well. So the proposition would have to be that if they’re there, they’ve got a function” [MJS]

How do you think his fellow-Darwinist scientists received his assertion (1987) that “Junk DNA” had a function? Read on the transcript:

“When I showed the professional geneticists the data, which indicated to me that the 95% non-coding region wasn’t junk, and was ordered…The reaction was smiling disbelief at best — you’re off your friggin’ head and if you’re any good at squash — stick to your day job” [MJS]

(For those asking, I may give you a copy for your personal perusal of the video that you would never in your life forget — especially if you or your loved ones encounter one the gezillions of “junk DNA diseases”. If you have gotten rich — and old enough that some of these regulatory diseases start popping up - your best investment may be to endow frantic research precisely for PostGenetics Centers. Probably unlike dear Malcolm himself, you might actually buy some years to live)

Thus, although when we are already re-entering the cyclone with an opposite wind building up with accelerating speed, “it is too easy” (and looks quite childish, though very human) to “back-pedal” in post-June 2007 on the issue of “Junk DNA”. Most everything is on record, already.

For instance, that it is probably the understatement of Genomics that science pioneers were doing so to get rich by going against dogma (dear Malcolm is anything but “materially rich”). He just knew that he could never publish in the establishment views branded (“framed”) as heretical views - tried to maintain his integrity, leadership and perhaps earn some living from those with dollar signs in their eyes buying up IP “on the cheap”. (Gregor Mendel got any rich? Rosalind Franklin? How about Barbara McClintock who stopped publishing rather than getting ridiculed by a majority of PR firing power but minority of intellectual marksmanship?)

Instead of engaging in a “blaming game” (that may not be the best use of time, unless you enjoy it), you may also wish to drop shouting over some arbitrary ideological trenches. Try doing some actual R&D towards the “Algorithmic Design” of the Genome. We are all united on that one — Malcolm and myself even published (yes, in peer-reviewed science journal…) experimental support “http://www.junkdna.com/fractogene/0[…]llionisz.pdf” of quantitative predictions.

Yes, FractoGene even passes “the Onion-test” at least as well as any competitor “Junk DNA theories” in our times of PostModern Genomics (PostGenetics).

When your “hypothesis” predicts everything the result is that it explains nothing. All of their supposedly predictions are a posteriori after real scientists have studied, researched, tested and come up with publications. Like grandma used to said; “after you see the dog’s [Enable javascript to see this email address.] you can tell is a male.” That is why ID is not science, it has no explanatory nor predictive powers.

Whereas optimal design demands a perfectionistic, anal-retentive designer who has to get everything just right, intelligent design fits our ordinary experience of design, which is always conditioned by the needs of a situation and therefore always falls short of some idealized global optimum.

This is typical of theistic intellectual dishonesty. Sure design is always conditioned by the needs of a situation, but that just means that optimality is locally defined, it doesn’t explain lack of optimality – what explains that is that the designers we are familiar with lack omniscience and omnipotence.

But such mechanisms cannot explain the complex, information-rich structures in nature that signal actual and not merely apparent design—that is, intelligent design.

Ah, but they can. Despite refutation after refutation of Demsbki’s work, he bleats on as if they had never been written. And throwing in the word “intelligent” explains nothing at all – intelligence isn’t some magic loophole through which the laws of physics, information, or logic can be avoided. If Dembski truly had a theorem showing the
impossibility of natural processes producing design, then we couldn’t produce any of the designs we produce. But, just as human intelligence arises from the actions of dumb molecules constrained by the laws of physics, so can
everything else we observe in the world, including the biological world. Despite the strongest possible illusion that
we are ghosts above and beyond our physical bodies, science has demonstrated in considerable detail that we aren’t. The claim to free will shatters when scientists can measure a decision being made in the brain before the subject consciously “makes” the decision, and when they can generate experiences, including “seeing God”, by poking appropriate places in the brain. It’s mechanism all the way down.

The good that God initially intended is no longer fully in evidence. Much has been perverted.

So much for omniscience, eh? And how did the world get perverted? Even if God created man with free will who then abused God’s intent, how does that explain the “perversion” of nature? Did man create malaria, or did God? Or does one go where evidence and reason lead and conclude that neither did.

the hard work of faith, whose job is to discern God’s hand in creation despite the occlusions of evil

Ah, yes, faith. Faith is what requires one to be intellectually dishonest, to ignore or pervert evidence and reason, whether on the grand scale of Dembski and the fundies or with lesser sophistries. Faith spawns apologetics, which is a euphemism for sophistry and dishonest argument. It goes directly against Quine’s dictum, a dictum that is so evident in the way that biologists have moved away from Mayr’s panadaptationism as the evidence has unfolded:

The desire to be right and the desire to have been right are two desires, and the sooner we separate them the better off we are. The desire to be right is the thirst for truth. On all counts, both practical and theoretical, there is nothing but good to be said for it. The desire to have been right, on the other hand, is the pride that goeth before a fall. It stands in the way of our seeing we were wrong, and thus blocks the progress of our knowledge.

It will take decades to determine what noncoding DNA does. It will never be answered by sitting on the sidelines and making noise which is the standard mode of operation for the DI.

The provisional simple minded answer right now is, some is functional, some is just there. We’ve rehashed this often, I posted a few threads ago for the third time, the mouse megabase deletion results which is at least novel empirical data.

Here is another recent experiment. Which indicates that some noncoding does something. What is interesting about this stretch of DNA, is that it codes for a common allele which raises the risk of coronary heart disease, the major killer in the USA, and was found by standard statistics linkage analysis. So far so good. But there is nothing in this stretch of DNA. No protein coding regions. No obvious small regulatory RNAs. Definitely a mystery and it could be a long time until it is known what it is about this stretch of DNA that raises the risk of CHD.

Coronary heart disease (CHD) is a major cause of death in Western countries. We used genome-wide association scanning to identify a 58-kilobase interval on chromosome 9p21 that was consistently associated with CHD in six independent samples (more than 23,000 participants) from four Caucasian populations. This interval, which is located near the CDKN2A and CDKN2B genes, contains no annotated genes and is not associated with established CHD risk factors such as plasma lipoproteins, hypertension, or diabetes. Homozygotes for the risk allele make up 20 to 25% of Caucasians and have a approximately 30 to 40% increased risk of CHD.

PS Wonder what the DI explanation is for the very ancient 8% defective retroviruses that make up the human genome? The ones that go back in the primate lineage 10’s of millions of years. On second thought, I doubt it would be very specific.

Are you male? Are you over 50? If so you shouldn’t need to ask. If not, well as someone once remarked, why run a waste disposal system through an amusement park?

Seriously, an enlarged prostate can cause many problems with excretory function. That’s because the excretory system runs right through the prostate. Not very intelligent design. And of course then there’s always prostate cancer to worry about. Every male over 50 should be screened regularly.

The following is an excerpt from Science Daily and it clearly explains the latest research finding on “junk DNA”.

“Science Daily — A tiny opossum’s genome has shed light on how evolution creates new creatures from old, showing that change primarily comes by finding new ways of turning existing genes on and off.

The research, by an international consortium led by the Broad Institute of MIT and Harvard, revises our understanding of genetic evolution. Scientists previously thought that evolution slowly changed the genes that create specific proteins. As the proteins changed, so did the creatures that owned them.

The current research shows that opossum and human protein-coding genes have changed little since their ancestors parted ways, 180 million years ago. It has been the regulation of their genes - when they turn on and off - that has changed dramatically.

“Evolution is tinkering much more with the controls than it is with the genes themselves,” said Broad Institute director Eric Lander. “Almost all of the new innovation … is in the regulatory controls. In fact, marsupial mammals and placental mammals have largely the same set of protein-coding genes. But by contrast, 20 percent of the regulatory instructions in the human genome were invented after we parted ways with the marsupial.”

The research, released Wednesday (May 9, 2007) also illustrated a mechanism for those regulatory changes. It showed that an important source of genetic innovation comes from bits of DNA, called transposons, that make up roughly half of our genome and that were previously thought to be genetic “junk.”

The research shows that this so-called junk DNA is anything but, and that it instead can help drive evolution by moving between chromosomes, turning genes on and off in new ways.”

Well, that should clarify things alot. How this can take either side of the evolution-creation debate is beyond me, though.

You asked this incredibly moronic question in a previous thread and it was pointed out by many people in that thread why it is immensely moronic. Why ask it again, if not to prove that you are stupid and dishonest?

No. Luskin is a very competent bait-and-switch artist. And the only thing that it “proves” is that he and his fellow IDers have no scientific alternative to evolution, and know it. If these scammers didn’t need YECs and OECs for political support they’d be saying something like “we have the real theory of evolution.” Of course it would still be pseudoscience.

Even if that were the goal, it wouldn’t make the post from Banned any less stupid.

Here’s a clue for you: people as transparently moronic and intellectually dishonest as you and Banned are (and you’re most likely the same person) cannot and will not convince anyone of anything. I’m sure such powerlessness must be frustrating for you. But just think of the glory that awaits for you in heaven when your pathetic useless existence on this globe ends.

Most IDists that I have heard/read are claiming that all or almost all will turn out to have “function.” The more religious ID types and even the not so religious types, will accept the proposal that “junk” DNA is due to the “post-Fall” state we are in. That is to say, at one time all this DNA had function and all us critters were created perfect… but since the “Fall” we now have some de-activated and/or corrupted stuff in our genomes. Anyhow… that is how the story goes.

Relatively recently I think the IDists have been downplaying or ignoring the earlier “post-Fall” explanation for two reasons:

1. Pinning the reason for “junk” DNA on “the Fall” is definitely an explanation tied to religion. They are trying to avoid mixing up their “scientific” ID with any specific religious content. This is only politically expedient for them at present.

2. As always, IDists do no actual science in support of their movement, instead they snipe and cherry pick at real science done by real scientists from the sidelines. This behavior is especially targeted at the branches of science and fields that are making rapid progress, which is exactly what is going on with genomics at the moment.

The IDists are really that desperate. I think that deep down they understand that they don’t really have any real science that they can do. For their intended audience, it is enough that they call real scientists the pig fuckers and let them do the denying.

You asked this incredibly moronic question in a previous thread and it was pointed out by many people in that thread why it is immensely moronic. Why ask it again, if not to prove that you are stupid and dishonest?

“Relatively recently I think the IDists have been downplaying or ignoring the earlier “post-Fall” explanation for two reasons:”

You make some excellent points. Please allow me to add another reason why the “Fall” scenario is unfeasible.

3) Several “junk DNA” features are shared with Chimpanzees and other primates, such as retroviral transposons inserted into specific genes. Obvioulsy the “Fall” cannot possibly explain such shared features.

David (Stanton) is correct. The main reason why neither IDists (except perhaps the token few who genuinely accept common descent) nor “traditional” Creationists can accept the idea of “junk DNA” is that non-functional DNA features shared between species are prima facie evidence of phylogenetic relationship.

The main reason why neither IDists (except perhaps the token few who genuinely accept common descent) nor “traditional” Creationists can accept the idea of “junk DNA” is that non-functional DNA features shared between species are prima facie evidence of phylogenetic relationship.

Exactly. Much like the argument from Evil for the theists, the argument from Junk (especially shared junk) is simple and devastating for the IDists. They must therefore resort to the same twisted apologetics to convince their audience that “[the Designer] works in mysterious ways”. Their attempts range from “who are we lowly humans to say it’s junk?” (for audiences favouring a simplistic, literal interpretation of [a Designer]) through to the “who are we to say what [the Designer] would or would not do?” (for those sophisticated theological sorts who are willing to reinvent [the Designer] to fit the data). It’s no surprise that Luskin is so obsessed with junk DNA.

Having worked in an investigative capacity for years at a previous job, as a seasoned investigator, I realized that sometimes; even when all evidence pointed toward one thing; sometimes that evidence, in the final analysis, summed up to something entirely different than we had originally conceived.

Wow, that’s what you learned? That’s the depths of banality.

In dismissing God at this early stage of our genome intrepetation,

Too bad you know nothing of science. God isn’t dismissed, for God isn’t even introduced by any evidence. If you’re an investigator, you’re a pathetic one, since you have no business bringing up “possibilities” which have no evidence for them.

Should you ever find evidence for God, present the evidence. That’s all we demand of IDists, and they never present any real evidence.

we are not even giving him the chance that we, as Americans, would give a citizen in a court of law.

I suppose that’s because we don’t know that he exists. How bright are you?

I know you guys will be screaming as you write, insulting me with your poison key pads :) -

You claim to be bringing up something new (God hasn’t been disproved by science), when virtually all of us acknowledge this fact. Learn something about your interlocutors before you decide to grace us with the wisdom of your trite and banal cliches.

and why will you be doing this?

It’s because it’s a very stupid and old PRATT (point refuted a thousand times), and has nothing to do with the statements made by science.

Because you know, deep down inside, that I am right.

Because it means as much as the fact that we can’t disprove that a teapot orbits Mars, to use Russell’s famous example. IOW, you’re trivially right, and there’s not the slightest reason we should care about that fact.

Perhaps as an investigator you’re incapable of noticing that we’re discussing what’s appropriate in science, not whether or not God exists. Just because ID is really only concerned with the latter issue doesn’t mean that we’re generally interested in that fact at all. What we’re concerned about is what any decent investigator is interested in, following the rules of evidence to the best conclusion possible at a given time. And at this time the conclusion that God had something to do with the genome is wholly unwarranted, for nothing in it differs from what “natural processes” would be expected (given our state of knowledge) to produce.

I’d like to see you try to bring up the fact in court that it is impossible to show that God tampered with the crime scene. You’d be laughed out of court, because that’s so obviously true and unimportant to the case that only an idiot would bring it up.

Dr. Pellionisz:
before you get people to do the hard work for you, you must make predictions that are not as shifty and ambiguous as you have done so far, to make it worth the while. Let’s start with these 3:

- If one provided actual species, their genome’s C-values, and some objective measurement of Purkinje cell morphology (in other words, much more information than provided in your fugu paper), what would be your prediction of the expected correlation? Be specific, please.
- Also, I am still trying to get you to commit to say something with regard to P-cells in lungfish, salamanders etc, which should really stand out with respect to P-cell arborization given their massive genomes. What do you think they look like? Will their arborization be, say, 10-fold higher than human? 30-fold?
- And if I gave you C-values of, say, 3 or 4 vertebrate genomes, could you align them in order of Purkinje cell complexity, without knowing the species beforehand?

You gotta give us something, otherwise it’s a pointless exercise. So far, the information Aryaman provided (several of the species names he provides are correct, by the way, and I have a few more) already clearly contradict your hypothesis, so you’ve got kind of a hole to climb out of.
There is actually a lot of information out there, although strangely almost none of it is included in your paper.

My heartfelt congratulations that we resuscitated your PT thread to the level of scientific cooperation, well under way with “protocol design”. This is really something! Such a phenomenon does not happen in every blog, though the scientific goal is (should be) identical in our PostModern times of Genomics (towards Post-ENCODE Genetics, PostGenetics).

I hope you realize that as in any algorithmic approach in PostGenetics, there is much more to FractoGene than the “minimum program of the Purkinje cell of the Danio” (that you deemed as doable swiftly). We wrote in the paper that “The Danio results … and other comparison are expected to blossom as a new branch of research”. I am happy that it really looks like this is the case.

Some “more global” answers will also be apparent from my deeper answer to Aryaman, but all PT bloggers should also be familiar with the “Onion Test” by T. Ryan Grigory - noting that the Purkinje brain cell is only one of the conspicuous platforms to FractoGene application. While the “Purkinje cell” prediction of FractoGene does not apply to the onion, the “Methylation Prediction of FractoGene” does.

Therefore, while with Dr. Simons we have already (from his viewpoint, quite heroically) pioneered the trail, for reaching highs of “full vistas” the types of “PostGenetics Centers” would ideally be required that integrate biology, statistics, computer science, mathematics, physics, and engineering and span from plants through bacteria to mammals, such as the undeclared but de facto emerging “PostGenetics Center” at Duke; www.junkdna.com/#duke_igsp

Since there is competition around, we better follow-up in private emails with specific plans. Nonetheless, abbreviated public answers to your 3 questions can be given as follows:

[AB] (1) “If one provided actual species, their genome’s C-values, and some objective measurement of Purkinje cell morphology (in other words, much more information than provided in your fugu paper), what would be your prediction of the expected correlation? Be specific, please”

As for specifics, I am sure you will correct your oversite that the “fugu paper” is closely coupled to my fractal modeling going back 17 years

fractogene.com/89_fractal/89_fractal.html

where I have long provided the “objective measurement of Purkinje cell morphology” (reducing “complexity” to levels of fractal hierarchy of e.g. a Lindenmayer-string fractal). If you (or others) would like to tackle e.g. the zebrafish P-cell, the “piece of cake” Golgi-staining might be entirely skipped to provide computer modeling of P-cells as I did since 1973, or like in more contemporary form; what DeSchutter et al. honed into a mastery: See #21 in the references of the “fugu paper”. Their prep was based on fluorescence-studies, concluding in a computer-reconstruction (of the guinea-pig PC), albeit they have not proceeded (yet) to fractal modeling and on. They might (have) at any time.

If even such a “laser-beam focused” mini-project is doable by an Assistant Professor in a Department of Medicine, you can tell better.

Since I suspect that you are determined to tie my integrity to integers, looking at my Figs. 3-4 in the “Fugu” paper, it appears that the Fugu (B in Fig. 4) is comparable to the “fractal template level” , while the Guinea Pig (E? — now established!) is comparable to the “fractal model, level 3” on Fig. 3). The Human PC is comparable to a level between 4-5 on the curve. (Sharply note that I did not imply “linearity”).

[AB (2) — “Also, I am still trying to get you to commit to say something with regard to P-cells in lungfish, salamanders etc, which should really stand out with respect to P-cell arborization given their massive genomes. What do you think they look like? Will their arborization be, say, 10-fold higher than human? 30-fold?”

No, I don’t think so. Andrea, are you also inclined to press me to commit myself to the P-cells in the Onion? — since the onion is part of what used to be the “C-value enigma”. In most (all) cases, we really don’t know if just one particular cell is the cause of the excess, and if that were the lucky case, which cell(s).

Sorry, the poor onion does not have a cerebellum (“invented” for the shark and on)… In science, one strives to find out first the rule (cf. Galileo’s planetary system centering NOT around the Earth) and then it is much easier to conclude on aberrations (e.g. finding Pluto).

If you insists on hearing my opinion on e.g. the Mormyrid P-cell (I know how they look like…), I don’t think that their level of fractality is high, at all. Since I happen to have a mathematical theory of the cerebellar function (TNT, yes, with predictions experimentally confirmed), I suspect that the electric fish operates its sensorimotor transformation not merely in the 4-dimensional Minkowski space-time manifold (under visual sensory control, as e.g. we do), but involving a much broader sensory-frequency-range (imagine including all ultraviolet and infrared domains of electromagnetic waves), and thus the P-cell needs a much higher number of parallel fibers (and thus, much higher number of granule cells) compared to cerebella at similar advancement in the phylogenetic ladder. Likewise, I don’t think that the exceptions in genome-size of lungfish, some frogs, different salamanders is likely to do either with the cerebellum in general (and thus, not with the Purkinje cell). It is much more likely, that these excesses reflect on the specifics of metamorphosis of various sub-species.

It is quite possible, however, thus well-worth of the chase, that we’ll succeed to “hit on a PC” with excessive fractality of one sub-species over another, and connect it directly to their differences in specific regions of (formerly) “junk DNA”. That will be a good time to open champagne. Kindly note that this rather deep question has to do with the “multifractal” as opposed to “monofractal” nature of vertebrate organisms. (I already have some leads on the onion, but, again, that can not involve any cerebella or Purkinje cells…)

[AB (3) — “And if I gave you C-values of, say, 3 or 4 vertebrate genomes, could you align them in order of Purkinje cell complexity, without knowing the species beforehand?”

If they represent “the rule”, yes. If they represent exceptions (see above) most likely not.

The “triangulation effort” is extremely important in either case. All blog readers will sharply note, that there are a good number of rather different cells in higher-order organisms (a “multifractal”). If development of the “trunk” or “hat” should “mushroom” in various cases, is exciting and useful target of research. Wherever there is a “peak” of excessive reverberate iterations (requiring, according to FractoGene, see also “Methylation prediction” the picking up of “auxiliary information lurking in what used to be ‘Junk DNA’”) I would immediately like to track it down “who — amongst the many - is/are singing such a long song”. This, however, will need tons of more Genomics (of the PostGenetic kind). At this point, we barely know even how the “genes” would “grow” a normal Purkinje neuron — let alone our very initial actual knowledge of the roles their intronic and intergenic regions play in physiological and/or pathological growth.

I said “very initial”. Of course, our knowledge is not equal to zero. For instance, the well-known intronic GAA triplet-repeat that is known to be the cause of the Friedreich Spinocerebellar Ataxia (a lethal hereditary syndrome, a veritable “Junk DNA disease”) has already been identified by FractoGem Miner as a fractal defect “in the junk” of X25.

There is a lot in any new approach. I am more than willing (delighted!) to share in proper formats.

[AB] (1) “If one provided actual species, their genome’s C-values, and some objective measurement of Purkinje cell morphology (in other words, much more information than provided in your fugu paper), what would be your prediction of the expected correlation? Be specific, please”

As for specifics, I am sure you will correct your oversite that the “fugu paper” is closely coupled to my fractal modeling going back 17 years

fractogene.com/89_fractal/89_fractal.html

where I have long provided the “objective measurement of Purkinje cell morphology” (reducing “complexity” to levels of fractal hierarchy of e.g. a Lindenmayer-string fractal). If you (or others) would like to tackle e.g. the zebrafish P-cell, the “piece of cake” Golgi-staining might be entirely skipped to provide computer modeling of P-cells as I did since 1973, or like in more contemporary form; what DeSchutter et al. honed into a mastery: See #21 in the references of the “fugu paper”. Their prep was based on fluorescence-studies, concluding in a computer-reconstruction (of the guinea-pig PC), albeit they have not proceeded (yet) to fractal modeling and on. They might (have) at any time.

If even such a “laser-beam focused” mini-project is doable by an Assistant Professor in a Department of Medicine, you can tell better.

Since I suspect that you are determined to tie my integrity to integers, looking at my Figs. 3-4 in the “Fugu” paper, it appears that the Fugu (B in Fig. 4) is comparable to the “fractal template level” , while the Guinea Pig (E? — now established!) is comparable to the “fractal model, level 3” on Fig. 3). The Human PC is comparable to a level between 4-5 on the curve. (Sharply note that I did not imply “linearity”).

OK, I take this to be your statement that an objective measure of P-cell fractal properties, using a suitable methodology (e.g., from a peer-reviewed paper), in a suitable series of organisms (vertebrates, of course, with genomes of not particularly unusual size - see below) should positively correlate with their genome’s C-value? Can we finally nail down this prediction of yours, and move on to test it? A simple yes or no will suffice.

[AB (2) — “Also, I am still trying to get you to commit to say something with regard to P-cells in lungfish, salamanders etc, which should really stand out with respect to P-cell arborization given their massive genomes. What do you think they look like? Will their arborization be, say, 10-fold higher than human? 30-fold?”

No, I don’t think so. Andrea, are you also inclined to press me to commit myself to the P-cells in the Onion? — since the onion is part of what used to be the “C-value enigma”. In most (all) cases, we really don’t know if just one particular cell is the cause of the excess, and if that were the lucky case, which cell(s).

Sorry, the poor onion does not have a cerebellum (“invented” for the shark and on)… In science, one strives to find out first the rule (cf. Galileo’s planetary system centering NOT around the Earth) and then it is much easier to conclude on aberrations (e.g. finding Pluto).

If you insists on hearing my opinion on e.g. the Mormyrid P-cell (I know how they look like…), I don’t think that their level of fractality is high, at all. Since I happen to have a mathematical theory of the cerebellar function (TNT, yes, with predictions experimentally confirmed), I suspect that the electric fish operates its sensorimotor transformation not merely in the 4-dimensional Minkowski space-time manifold (under visual sensory control, as e.g. we do), but involving a much broader sensory-frequency-range (imagine including all ultraviolet and infrared domains of electromagnetic waves), and thus the P-cell needs a much higher number of parallel fibers (and thus, much higher number of granule cells) compared to cerebella at similar advancement in the phylogenetic ladder. Likewise, I don’t think that the exceptions in genome-size of lungfish, some frogs, different salamanders is likely to do either with the cerebellum in general (and thus, not with the Purkinje cell). It is much more likely, that these excesses reflect on the specifics of metamorphosis of various sub-species.

Well, I did not mention onions at all here. Indeed, onions, amoebas, and thousands upon thousands of other organisms with very large genomes do not have cerebella, which is kind of a snag for your model. But anyway, while I take notice that you now agree your hypothesis does NOT address the “onion test” after all, what I really was getting to was vertebrates. Indeed, vertebrates that are phylogenetically closer to mammals than fugu is. (Invoking metamorphosis seems rather ad hoc, frankly, since most organism that undergo metamorphosis do not have particularly large genomes. You are not claiming that DNA fractality is generally associated with metamorphosis, right?)

Regardless, by refraining from making any prediction in this case, I assume you are saying your model does not apply to vertebrates with unusually large genomes either. In other words, it can pass neither the “onion test” nor the “lungfish test”. Although it’s unclear to me why the model should still apply to vertebrates with unusually small genomes (like fugu), I’ll take you at your word, and move on.

[AB (3) — “And if I gave you C-values of, say, 3 or 4 vertebrate genomes, could you align them in order of Purkinje cell complexity, without knowing the species beforehand?”

If they represent “the rule”, yes. If they represent exceptions (see above) most likely not.

Well, then, what is the rationale for considering some organism a “rule”, and another an “exception”? Why isn’t fugu, or zebrafish, an exception? Why isn’t lungfish the rule? You gotta be more specific on this, before we proceed.

“I fail to grasp the rationale behind focusing on the morphology of the Purkinje cell, other than the fact that Mandelbrot said it looked like it was fractal and could be amenable to analysis using non-Euclidean geometry. So what?”

“I have no problem with the idea that some sort of scaling or power laws or fractal dimensions may be involved in animal morphology and metabolism (In fact, I really like some of the work in this area…)

[AJP] I composed a “longhand” answer, but in reference to the last and most fundamental comment I would really like first to know the feedback from Aryaman to the article (and my comments) at:

The first (“why Purkinje”) is a good question, since Aryaman (unfortunately for his interests) failed to grasp the important rationale of picking the Purkinje neuron as an excellent, perhaps the best, “platform” for “triangulation of genomics, morphogenesis and biophysics”. (There may be an “Onion cell” equivalent to Purkinje and/or Red Blood Cells — neither existing in plants. I have some leads but the story is not ready to print).

The second (“so what”) is also a pithy question, though a bit unnatural and quite foreign to Aryaman, as it sounds as a crudely phrased red-neck “bottom-line” question, like “what is in it for me?” “So what if we find non-Euclidean geometrical laws governing DNA structure and function”? Decide for yourself…

The last comment is by far the most important; “mathematical scaling laws ruling morphology and metabolism”.

Starting with the most important, it seems too bad that those obsessed with the “rule of random” usually are not very mathematically minded. This is a problem for biology. When mathematics becomes a barrier rather than an invitation, what you usually get is a lot of data — yet little understanding.

Since Dr. Shalizi knows a few things about cerebella, it is mostly for other bloggers to mention that the Purkinje neuron (of the cerebellum) is usually the biggest kind of brain cell. Why is that important? For instance, because of his most substantial comment (“metabolism”). It should strike learned bloggers that both the red blood cells that show best the correlation with C-value, as well as the Purkinje cells, are “metabolically distinguished”. However, it should also be clear to the mathematically minded (as pointed out in our paper) that “most animals are not a single monofractal, as appears to be the case in some simple plants, but are almost certainly multifractal. This seems evident from the different fractal properties of their separable organelles (lung, coronaries, intestines, etc.) Therefore, the FractoGene concept might have to be augmented with novel methods of sequence analysis” (after publication signaled in www.fractogem.com and www.fractoset.com).

Aryaman further asks:

What does FractoGene … predict
[1] about other kinds of neurons? What predictions does it make about the relatively invariant morphology of, for example, cerebellar granule neurons, the single most numerous class of neurons in the central nervous system, which have an almost invariant morphology in all species that have cerebella? What predictions does FractoGene make about the structure of cortical pyramidal cells, which also show a much lower degree of morphological variation?

[AJP] See “Methylation prediction of FractoGene” — it is not limited to Purkinje neurons at all.

[2] about biological structures that do NOT have a fractal-like appearance?

[AJP] First of all, that it may be worth looking if the appearance is NOT OBVIOUSLY fractal-like, nonetheless hidden fractal properties (and rules) may be lurking beneath… (People who already swung to the other extreme from “what a nonsense” to “everybody knew all along it was fractal”, usually ask me: “tell me one thing that is NOT FRACTAL in Nature”… Same story, different attitude…)

CONSEQUENCE: It is unlikely that the Purkinje cell causes the excess in lungfish, frogs, salamandra, etc. but very possible that the Purkinje cell growth, as an illustration of the RULE, might be found in some sub-species as excessively slow to build (EXCEPTION).

LESSON: If one wants to go for the “quick and easy”, do the zebrafish PC (“satisfaction guaranteed, or your money back”).

OK, I take this to be your statement that an objective measure of P-cell fractal properties, using a suitable methodology (e.g., from a peer-reviewed paper), in a suitable series of organisms (vertebrates, of course, with genomes of not particularly unusual size - see below) should positively correlate with their genome’s C-value? Can we finally nail down this prediction of yours, and move on to test it? A simple yes or no will suffice.

You replied with 255 words, saying nothing to the effect that you are going along with this prediction. Do you? Don’t you? The advantage of this is that the data are already publicly available, so we could get an answer right away. Please provide a straight reply.

As for your comment, I still don’t get it: assuming nobody knows what Purkinje cells look like in salamanders and zebrafish, what is the actual, rational basis for your claim that salamanders will be the exception, and zebrafish the rule, to your prediction? This is crucial: let’s say we do the experiment and find that, contrary to your prediction, zebrafish have primitive PC arborization, and salamanders ultra-developed arborization, what will prevent anyone from then claiming that zebrafish must be the exception, and salamanders the rule?

Again, this is important with regard to the 3rd prediction highlighted above: if you tell us what makes an exception and what a rule, we can exclude the exceptions beforehand and just focus on a set of organisms that should, according to this yet unstated parameter, conform to the rule, and see if they indeed do.

I am trying to flesh out your predictions in an empirically testable fashion, but you don’t seem to budge.

Just because this thread is yours and I am a guest I don’t think you should feel entitled to interrogate me in a manner demanding “yes or no” answer to what is your re-phrasing of what I said. When quoting me, after you say “I take this to be your statement” please kindly apply a full stop. Rather not re-phrase, if you can resist.

From plenty direct communications I am getting, it is clear to me that most people agree with your (correct) opinion that Golgi-testing the zebrafish (Danio) PC is an easy game — and thus will be done swiftly (though for reasons I will not touch on in this public posting, most likely not by you).

In fact, our “Fugu paper” stated that:

“…we were curious to examine P-cell presence and dendritic complexity in Fugu and Danio. That study is to be reported separately (33). The authors have permitted us to refer to their results as “unpublished observations” for the Fugu. The Danio results (only partially available) and other comparisons are expected to blossom as a new branch of research”. [Fugu paper]

Readers will appreciate, however, that (especially regarding “other comparisons”) there is much more to a proper study by a Hungarian-Japanese joint program than coming up with a Golgi-stained Danio P-cell (as a preliminary result, I have seen *that*). Readers might come to the conclusion on their own (thus, after a sufficient lead-time, I don’t have to unduly jeopardize their publication priorities) that actually *two* curves have to be first plotted, and after curve-fitting (the customary way to tell apart what is “rule” and what is “exception”) the curve of the C-values of sequenced genomes along the emergence of species and the curve of “bifurcation levels” of the fractal models of P-cell over the axis of same sequenced species need to be compared. An appropriate time to open champagne is when particular species (in even luckier cases, sub-species) are found that yield exception in *BOTH* curves.

After the champagne will come some additional and even harder work - to plunge into genomic analysis of the P-cell of “particular (sub) species”. The latter is not totally unlike in the paper *you* appear to be a co-author, see your Fig. 3:

www.pnas.org/cgi/content/full/97/7/3336

but in reverse, what physiological *OR* pathological genomic causes may lie beneath an exception. (What FractoGene could help with interpretation of your data goes way beyond the limits of a blog).

Contrary to your superficial notes, exceptions both in the positive and negative domain are most significant. The positive excesses will substantiate not only the proposed explanation by PROCESS but also actual species to pin down the culprit cell(s) for excessive reverberate iteration (onion, salamandra). Negative excesses may indicate unduly “stuck” (pathological) recursion. When considering that such cell(s) may or may not be best found for PC-s, the above program is obviously of substantial size, since it may span from P-cells of vertebrates to cells of plants (onion). Since the full protocol entails morphology, fractal modeling, bioinformatics, physiology, pathology and genomics, as mentioned earlier, the entire project is best suited for a “Center of PostGenetics” (similar to the quoted new Ctr at Duke).

There is much more to planning a protocol (especially in competition with an ongoing one…), thus to protect interests my preference is direct communication - unless one enjoys posturing under pretexts of a (not so) hidden agenda.

Andras, you’re waffling. Andrea’s question was very fair, and very pertinent to the discussion. Until you answer it, you have effectively proposed an unfalsifiable theory, with all possible results being acceptable. We don’t like those much around here.

So please, in a nice, succint, answer can you please respond to Andrea’s question? Or shall we lump you in with all the snake oil merchants that come through this site?

You don’t seem to be a scientist. Do you think we in a “Kangaroo court” with the infamous “did you stop beating your wife, answer with YES/NO?”- types of “fair questions” by lawyers trying to nail true scientists? Scientists accept all experimental data — and define their role not to arbitrate the facts but explain them.

“demaillien”, what the heck do you mean by a “criticism of a scientific theory” for which “all possible results [are] acceptable”??? If a theory does not accept all experimental results (e.g. rejects proof of obvious non-randomness and by ignoring evidence continues to pretend that the vast majority of the DNA is “Junk”), in my eyes is not a theory, but a dogma. Count in this thread entries still denying role to “Junk DNA” beyond ENCODE evidence to the contrary. We have sadly witnessed what “kindergarten debates” ensue if e.g. this thread is based not on science but dogmatism in PT.

Non-scientists can enjoy the only thing they are good at; “name calling” in PT (in that case, I don’t belong here). Scientists of PT (who can be counted on the fingers of a badly injured single hand) face a colossal dilemma. Accept *all* experimental data (and explain them!) and go wherever they take us (regardless of hidden or not so hidden ideological agenda) - or trivialize science to make room for ideology (but in that case “scientists” will lose their credibility in science).

Dr. Bottaro should know better from *his* own pieces of evidence in science that “Junk DNA” not being “junk” leads all scientists to far more pertinent, better questions than what emanates from his leaning to trivialization in PT.

Dr. Bottaro readily acknowledged that the “Danio-test” (as a first cut) is “doable by a grad student in less than a week”. Why doesn’t he “just do it” but let others lead science studies?

I have two explanations, one should remain not declared. The other is that knowing his paper (cited above) I purposefully mentioned the FractoGem as a fractal defect in the intronic region of the X25 gene, as a cause of a well-known “Junk DNA disease” of Friedreich’ Spinocerebellar Ataxia.

Dr. Bottaro’s cited paper shows (his Fig. 3, bottom right corner of panel D) a gross dendritic aberration of a Purkinje cell in their paper on Ataxia Telangiectasia (another “Junk DNA disease”). Given the scientific importance of the topics (both FSA and AT), instead of leaning towards trivialization, IMHO Dr. Bottaro would have publicly (or, more likely, via private e-mail) wonder about the possibility if AT as a “Junk DNA disease” may be caused by a similar fractal defect as in the case of the Friedreich’ Spinocerebellar Ataxia - if he was serious.

Because an answer to the “so what about FractoGene” (applied to cerebellum, etc) question of Dr. Aryaman Salizi may, for any of us, be a life-or-death matter, see

www.junkdna.com/junkdna_diseases.html

(while the sheer fractal appearance of the dendritic arbor of the Purkinje cell is something that most people are justifiably unlikely to care about).

I have provided not a trivialized “one curve” but a more appropriate experimental protocol of *my theory* of “two curves” (with “rules” and “exceptions” according to customary curve-fitting). Too bad (for them) that non-scientists might not understand even the basics. Great for scientists who are already on their way towards novel and clear goals.

Well, speaking as another non-scientist, I don’t see how establishing that a stretch of DNA has a fractal pattern would establish that it also has some function. Fractal patterns as I understand them are caused by repetitive additions or insertions, which could be random (i.e., genetic drift). But I suppose I could be missing something.

(Of course, fractal by random addition could still (afaik) cause genetic disease, since for something to cause problems doesn’t necessarily require that it had a useful function prior to causing the problem.)

It is great to have bona fide non-scientists around, to explore how people think about “junk DNA”.

In principle, you are quite right to guess that “for something to cause problems doesn’t necessarily require that it had a useful function prior to causing the problem”.

I can answer using your earlier posting “…with more space there’s less detrimental effect of having unneeded stuff, so more junk accumulates” (to which somebody answered not to invite you to his garage).

Sure, you can have stuff crowding your garage that never served “useful function”. In practice, however, under Darwinian theory, you should then expect to drop out with your jeopardizing excess of junk (e.g. drop dead as you trip over stuff, or at least pay painful mortgage for space you can’t use); see Darwinian argument in 1987 by Malcolm J. Simons that compelled him to obtain his patents.

Since Malcolm is widely known to be affected by a “Junk DNA disease” himself, after having pinned down that “junk was anything but” he is motivated having already spent two decades to finding out the best approach to what might exactly be the function that Darwinian theory actually required.

Re “In practice, however, under Darwinian theory, you should then expect to drop out with your jeopardizing excess of junk […]”

Yeah, if reproducing the junk uses up a significant amount of resources, or if the junk interferes with some function - which apparently it sometimes does, but also apparently not all that often?

Presumably there’s a balance in there somewhere, natural selection removing actual junk, vs. insertions, duplications, and maybe other mutation types, adding it. I guess the question is where does one expect the equilibrium between those to be reached, and how quickly.

“Yeah, if reproducing the junk uses up a significant amount of resources, or if the junk interferes with some function - which apparently it sometimes does, but also apparently not all that often?

Presumably there’s a balance in there somewhere, natural selection removing actual junk, vs. insertions, duplications, and maybe other mutation types, adding it. I guess the question is where does one expect the equilibrium between those to be reached, and how quickly.”

[AJP] “How quickly”??? - How about not even in half a Billion years?

“Ultraconserved elements” are among the strongest arguments that if mother Nature did not drop out “junk” - they are likely to have function, e.g. to play key regulatory roles in vertebrate gene expression.

Just for one example, see the non-coding sequences conserved over half a Billion years (picture is worth a hundred word):

“We generated ~1.4x genome sequence coverage for a cartilaginous fish, the elephant shark (Callorhinchus milii), and compared this genome with the human genome to identify conserved noncoding elements (CNEs). The elephant shark sequence revealed twice as many CNEs as were identified by whole-genome comparisons between teleost fishes and human. The ancient vertebrate-specific CNEs in the elephant shark and human genomes are likely to play key regulatory roles in vertebrate gene expression”

Don’t blame me for such a finding and interpretation. The last 3 of the 12 authors were:

Re “[AJP] “How quickly”??? - How about not even in half a Billion years?”

That was how quickly would the two opposing effects reach equilibrium. Not how quickly natural selection would it wipe out unnecessary DNA sequences; if various effects are continually generating more such sequences, it won’t.

I don’t doubt that there’s some function in sequences for which function was not previously known; as far as I know, nobody expects that all functional sequences would have been identified already.

“I don’t doubt that there’s some function in sequences for which function was not previously known; as far as I know, nobody expects that all functional sequences would have been identified already”

Perfectly agreed. We rest our case.

Henry seems to be a very good (“fast converging to the facts”) case where even a “non-scientist” is likely to be convinced by hard evidence, that e.g. himself or a loved one, if suffering from a “junk DNA disease” should be helped by fast accelerated R&D in this field - regardless of ideology.

Andras,
Again, rather than answering the relatively simple question that Andrea has put to you, you chose to waffle and blither. Not a good sign.

What I don’t get is that you have come here to try and convince us by argument. We’re all rather more inclined to the scientific way of doing things here. You know, hypothesis, experiment, conclusion. I would expect that any scientist when faced with disbelief of his/her theory, would simply go out and do the necessary experiments to show that the theory is true (or false, if the doubters were right). You on the other hand try to convince people by badly expressed argument. That dog won’t hunt.

So, Mr Arrogant, go away, do some work, and publish the results. We might be more convinced by your stories afterwards.

Anyway, I don’t get what your point is. Although I am no biologist, I use genetic algorithms for my work, and have studied my Kimura and Kauffman, more so than you by all evidence. I certainly don’t know where anyone would get the idea that “junk” DNA had no purpose (ps, I thought that scientists had decided “junk DNA” was no longer the preferred expression). Genetic drift in particular would be impossible without it, and yet Kimura has shown the importance of this mechanism to evolution.

Furthermore, if rather than being an arrogant know-it-all, you had instead done some basic research on the various positions of commentators on this blog, you would know that we often regret the existence of the term “junk DNA”. You see, each time someone discovers some function in “junk DNA”, the creationists go wild, claiming, just as you do, that this disproves Darwinian evolution. And each time we have to explain that “junk DNA” just meant that the DNA in question doesn’t code for proteins, not that it can’t have any function whatsoever.

Please Andras, fell free to pull you head out of your arse, and go and do some work so that you can at least clearly respond to some of the more obvious question marks that hang over your theory. Until then, I for one shall be filing your word salads under the heading “snake oil merchant”.

Anonymous “demallien” wrote (readers will note that he/she is the last remaining “name-caller” comfortably hiding behind anonymity):

“…if … you had … done some basic research on the various positions of commentators on this blog, you would know that we often regret the existence of the term “junk DNA”..”

[AJP] It did not escape my attention that “Junk DNA” as a scientific term, that finally collapsed with ENCODE, will ruin all those who used it as a shield of mud-throwers. Many are still stuck underneath the rubble and keep exercising a kindergarten behavior - perhaps because of the trauma. “Demaillien”, don’t you realize that people are dying of “junk DNA diseases” while you still engage in hardly anything better than “name calling” at the level of a 5-year old child? Have you got any decency left? Why don’t you have the guts to say “yes, not only I regret the existence of the term “Junk DNA” but I am sorry that I am still in the way of those who rush to help those suffering from “Junk DNA diseases””?

Anonymous “demallien” says:

“I don’t get what your point is. Although I am no biologist, I use genetic algorithms for my work… I certainly don’t know where anyone would get the idea that “junk” DNA had no purpose (ps, I thought that scientists had decided “junk DNA” was no longer the preferred expression).”

[AJP] Now we are talking. (See, you could do a whole lot better than childish name-calling).

I am - in addition to a “PostGenetics Evangelist” here on PT - also one who pioneered Neural Networks (in an earlier paradigm-shift; you may have still been in the real kindergarten when I already did quite a bit of R&D, now turning to its 5th decade.. why don’t you check out the accomplishments of those that *you* criticize?)

Thus, I know quite well that workers of “Genetic Algorithms” are very well in tune with, and shall profit from, my efforts towards “Algorithmic Design to DNA approach”. “Genetic Algorithms” (yes, there are “fractal genetic algorithms”) together with Neural Networks will do wonders on the scorched land of what used to be “Junk DNA” - the 98.7% of human genome. Why don’t you discover the great opportunity (“don’t bite my finger, look where I am pointing”)???

I am proposing that all those under the shattered remnants of “Junk DNA notion” could escape to “Algorithmic Design of DNA”. It is something that even *you* can better use than to be stuck with those still crying “Junk DNA” and throwing mud on those who actually help getting over your problem.

Since you are “no biologist” it does not surprise me that you are ignorant not only of my accomplishments, but apparently never even read Dr. Ohno’s 3.5 page short abstract “So much junk in the human DNA” (1972) originating the concept that we have just buried. Kindly take the time to read the “Obituary of Junk DNA” at

Scientists accept all experimental data — and define their role not to arbitrate the facts but explain them. … Scientists of PT … “scientists” will lose their credibility in science

Your attempts to high-jack all sorts of scientists as being representative of biology is revealing of your motives, as is your attempts to turn away the discussion from moving beyond untested suggestions of correlations.

The biologists among us know the facts, and we want to use them to arbitrate the explanation (theory). You have had room to explain yourself at length, but when Andrea Bottaro challenge your theory to give a simple prediction you feel interrogated. You seem to feel it is about your oh so important to guard research, while it could as well be tests with known data.

You even feel so threatened that you unfairly label Bottaro’s question as unscientific when it is repeated by non-scientists. (Again, the intentional confusion - you mean not knowledgeable biologist.)

The impression you give is that your theory can’t answer simple questions that data should explain. If that is the impression you want to make here, fine. Just don’t go around in the process and throw around silly and erroneous characterizations of other scientists and sciences.

(Oh, and stop jumping on laymen members of the blog discussion - this blog is for all interested, and not acknowledging that makes your efforts seem silly there as well.)

1) Junk DNA as non-functional stuff is history
2) Anyone of us can get sick or die because of “Junk DNA” glitches
3) Those clinging to the notion of useless Junk (scientists or not) don’t do us good service — and badmouthing is an outright disqualification
4) There are algorithmic approaches to explain function beyond 1.3% (“beyond genes”)
5) “Simple tests” for a leading one can be done in 1 week by a grad student (zebrafish PC)
6) Testing and refining competitive approaches will take significant resources and time and thus intellectual property is, and increasingly will be, a key factor

Specialists in the field already know:

1) Designing competitive research protocol is not a blog issue. Peer-reviewed science publications are appropriate public means, while already ongoing and developing collaborations are arranged directly
2) PostGenetics Centers are emerging (declared by name or not). Challenges are interdisciplinary and collective efforts are a must
3) The PostModern era of Genomics is disruptive, its birth is painful and entropy of the emergence is high. Pioneering, by definition, takes a lot of flak - what else is new?

1) Junk DNA as non-functional stuff is history
2) Anyone of us can get sick or die because of “Junk DNA” glitches
3) Those clinging to the notion of useless Junk (scientists or not) don’t do us good service — and badmouthing is an outright disqualification
4) There are algorithmic approaches to explain function beyond 1.3% (“beyond genes”)
5) “Simple tests” for a leading one can be done in 1 week by a grad student (zebrafish PC)
6) Testing and refining competitive approaches will take significant resources and time and thus intellectual property is, and increasingly will be, a key factor

And arrogant PhDs that are full of themselves will remember that science doesn’t care about titles, it cares about good ideas. I can’t help wondering if Andras would have rejected Einstein’s work out of hand - after all, what would a “lay person” working in a patent office know abut physics, right? On the other hand, as Andras has apparently discovered [snicker], a PhD won’t protect bad ideas from criticism. This is as it should be.

Specialists in the field already know:

1) Designing competitive research protocol is not a blog issue. Peer-reviewed science publications are appropriate public means, while already ongoing and developing collaborations are arranged directly
2) PostGenetics Centers are emerging (declared by name or not). Challenges are interdisciplinary and collective efforts are a must
3) The PostModern era of Genomics is disruptive, its birth is painful and entropy of the emergence is high. Pioneering, by definition, takes a lot of flak - what else is new

So why are you here boring and insulting us Andras? If blogs aren’t the appropriate forum, feel free to go elsewhere.

I note, in passing, still no data to back up the claims. Still no courage to predict what those experiments would show. Snake. Oil. Merchant…

By the way, could you please, for the love of FSM, stop repeating the strawman that science thinks that “junk DNA” has no purpose. It hasn’t been true since Kimura, which was when? 1960s? No-one here thinks that junk DNA has no purpose, no-one of a scientific inclination has thought that for a very long time, so give it up already. You won’t convince us, because we’re already convinced by the data.

Speaking of data, when are you planning on giving us some. Or even just an answer to Andea’s question would be nice. Should be easy for an expert like you, come on, amaze all of us dumb “lay people” with your PhD brilliance…

Anonymous “demallien” and others still engaging in name-calling (with their hideous behavior nothing to lose) may wish to see my point: “badmouthing is an outright disqualification”.

Better yet, heed the warning by the owner of this thread:

–
Posted by Andrea Bottaro on July 20, 2007 9:33 PM (e)

People, this thread is depressing. Either you try to lift the tone above kindergarten-level name-calling, or I’ll just close it. It is sad that trolls can so easily derail a discussion here. They must be having a ball at our expense.
–

This thread fulfilled its role, anyway, since “Junk DNA as a scientific term is dead”. Long live PostGenetics; algorithmic design approaches and competitive concepts, let’s go ahead and do something for those suffering from “Junk DNA diseases”. The 60 (named) Founders and members from 34 Countries of International PostGenetics Society is a much better company with a positive agenda:

I used “hideous” according to its definition in the Merriam-Webster dictionary: “morally offensive”.

“Anonymous name-calling” (latest by “demallien”) in itself clearly falls into such category, IMHO. Those attempting to anonymously impugn the integrity of others backfires as it is only a reflection on those without merit to their “debates”. Kindergarten style is acceptable in a kindergarten but it depressed even the blog thread owner. Name-calling IMHO should be discouraged, (I credit this PT thread that it has been, not only by me), and is particularly objectionable when applied anonymously and in the interest of blocking or hindering efforts to help those uncounted millions suffering from “Junk DNA diseases”. Some of them may prove to be less forgiving than others.

Dr. Pellionisz:
it is obvious, and too bad, that you are unwilling to subject your hypothesis to meaningful testing. I do see why, however, since there is already considerable data out there that does not conform to your predictions. In addition to the data and links provided above by Aryaman Shalizi in a comment above, I will just point out to another interesting tidbit, in the paper by TG Smith et al, “Quantitative Phylogenetic Constancy of Cerebellar Purkinje Cell Morphological Complexity”, J Comp Neurol 331:402-406, 1993. It reports the quantitative analysis of Purkinje cell fractality in a number of placentates, one marsupial and two bird species, showing that fractal complexity is essentially identical in these species. C-values varies in these critters by about 3-fold. I found this paper particularly informative because it used objective quantification of the parameters in question, as opposed to just showing examples of supposedly representative P-cells (which of course raises the issue of observer bias, statistical significance, etc).

Anyway, to be entirely frank, in addition to your unscientifically secretive and prickly attitude, and your tendency to misrepresent existing evidence (I see you are still mischaracterizing the significance of the ENCORE findings, even after we have gone through them point-by-point), it is clear that your hypothesis, devoid as it is of a mechanistic basis and of significant predictive powers with regard to the existing evidence, has a tough hill to climb before it is taken seriously, so I wish you good luck with those endeavors.

Oh, one more thing. You stated:

Dr. Bottaro’s cited paper shows (his Fig. 3, bottom right corner of panel D) a gross dendritic aberration of a Purkinje cell in their paper on Ataxia Telangiectasia (another “Junk DNA disease”). Given the scientific importance of the topics (both FSA and AT), instead of leaning towards trivialization, IMHO Dr. Bottaro would have publicly (or, more likely, via private e-mail) wonder about the possibility if AT as a “Junk DNA disease” may be caused by a similar fractal defect as in the case of the Friedreich’ Spinocerebellar Ataxia - if he was serious.

I am serious, and I don’t need to wonder: I can actually go to the existing database of AT mutations, and check them out myself (as can you, by the way, but apparently don’t). As far as I can see, all known mutations in the ATM gene affect protein expression or structure, causing amino acid substitutions or truncations.

I will leave the thread open until the weekend, in case you want to reply, but I agree with you that it has fulfilled its role. I am particularly pleased that you now agree that a strict interpretation of Darwinian theory would predict that “junk DNA” should not exist:

In practice, however, under Darwinian theory, you should then expect to drop out with your jeopardizing excess of junk

This was of course the very point of my original post: that the claim by Casey Luskin and other ID advocates that Darwinian theory is somehow directly responsible for the idea of “junk DNA” is sheer nonsense, historically and scientifically. At least we have clarified this point to everyone’s satisfaction. I hope you will send an e-mail to Luskin in this regard.

I agree that your depressing thread, though I did what I could to lift it, served out its useful purpose

1) With ENCODE, “Junk DNA” is out, dead as a doornail. You are simply wrong to have said “*all* that anyone can conclude from the ENCODE data is the bare fact that more of the genome undergoes transcription than we suspected”. This insults not only all who took part in the 11-Country effort (for 4 years), but also flabbergasts those who now may wonder “is that *all* we spent $50 M tax-dollars for?”

2) Algorithmic Design approaches to DNA are in.

(Blog-alternatives were notified of these predicted outcome with my posting that eventually was made room here; Comment #188856)

I further agree that anything mathematical has a tough hill to climb with non-scientists, and even with non-mathematically minded biologists. I encountered in PT just a single person who knows a related field “Genetic Algorithms”, and even he/she preferred anonymous name-calling over actual science.

Your comments (as a scientist, but apparently short on mathematics) on the cited TG Smith et al. (1993) paper reveal your lack of understanding even basics of fractals.

You confuse “fractal dimension” with “fractal complexity”.

They are *not* the same at all. For instance, the Koch-curve can have and increasing “level 1”, “level 2” … “level n” complexity (ad infinitum), yet its “fractal dimension” is preserved through all levels (1.26, see an exemplary link below).

When looking at the Purkinje cells in my fractal model at different stages (my Fig. 3. B, C, D, E in the “fugu paper”) those familiar with fractals know that their fractal dimension is preserved. This is a core concept to fractals; scale-free self-similarity (“pattern in a pattern”), based on the invariance of fractal dimension in the small or in the big. The TG Smith (1993) paper says exactly that (no more) for Purkinje neurons by a sampling of species (Dr. Shalizi did even less, he only guestimated 5 out 8 genome-sizes). It is too bad that TG Smith et al. having spotted a fractal property did not follow-up on towards any “fractal model” of one or more P-cells (though I published mine in 1989). I don’t blame them, however, the first “fractal wave” (from 1989 — to 1996) was likewise butchered (see refs. 15-16 in the “fugu paper”) as the “Operon-regulation” by Jacob & Monod in 1961 was derailed (in spite of their Nobel in 1965) by the deliberate framing of Ohno (in 1972). People often mistake “kindness for weakness” and “assertiveness for arrogance”, but masses at this time will rise for millions dying of “junk DNA diseases” and make this new wave break through. Clearly, fractal modeling was beyond TG Smith et al., and is apparently beyond you or Dr. Shalizi — but I went with Dr. Simons on record with peer-reviewed journal publication and I even outlined a program here that takes a collective effort for a PostGenetics Center).

Dr. Bottaro, with your present ignorance you will have to climb, however, mountains of mathematics before anything you touch upon fractals or FractoGene can be taken seriously, so I wish you good luck with the endeavor of catching up with the mathematical necessities to pursue PostModern Genomics.

[AJP] This is total nonsense. On the contrary, you and PT will remain on record that “it takes less than a week for a grad student” to come up with the zebrafish-test of FractoGene, yet PT is apparently unwilling to spend even a week of effort if evidence for Algorithmic Design is not in their perceived ideological interest. (Although I tried to help, since “random” and “junk” will lead PT nowhere - while it may still be time to embrace Algorithmic Design). We published with Malcolm Simons a peer-reviewed paper open to the whole World, with the declared invitation to rally experimentalists; “comparison are expected to blossom as a new branch of research”. In a provocative manner, we even placed unmistakable “question marks” to point where to look; and one question mark has been answered within two months (guinea pig genome size, right on target). You may label it “secretive” that I don’t give away in a blog progress reports that my colleagues and I actively cooperate with are doing, or that I don’t throw away my IP for blogs, but I think it would be less than smart to do that; you may not even be honestly asking.

Oh, one more thing.

Most fortunately, FractoGene (and in general, more-and-more mathematically minded approaches in PostModern Genomics) will be appreciated not by those who are ignorant of even the basics of mathematics.

Research will be judged by those who suffer “Junk DNA diseases”.

Yes, let’s take Ataxia Telangiectasia (ATM), in which you found Purkinje neurons truncated in their dendritic arborization. Thus one should, IMHO, wonder if ATM intronic mutation could be identified as a fractal defect of a regulatory mechanism. (Although I am quite familar with tabulations “under development” for genomic mutations, I just don’t think that staring at them, without some coherent conceptual framework of how the full genome works, will in itself result in actually helping patients).

Apparently, you may not have looked Vorechovský et al (1996) in www.junkdna.com/junkdna_disease.html

“We describe the first ATM mutation in the splice junction found in the 5’ splice site of intron 17, leading to exon skipping”

I submit to you (more so to learned parents of kids affected by this syndrome) that an intronic fractal defect, derailing regulation, might really be of the interest of those who are really serious.

Who are “really serious”? People affected with “Junk DNA diseases” and their loved ones! They will soon be outraged en masse that Genomics and Medicine before ENCODE was “barking up the wrong tree” (protein synthesis with Crick’s Central Dogma) — and R&D were not paying enough attention for non-genic(regulatory) mechanisms, such as fractal structures and their defects that FractoGem Miner can help identify.

It has been and will be interesting to chalk up giants of genomics one-by-one (who earlier went on record as “Ohno followers”) lately turning from the wasteland of “Junk-yard” to the riches of “Regulation Research” (Collins, Venter, Brenner, to name just a few). It will be increasingly embarrassing for the remaining hold-outs (Dawkins, some non-scientists in PT, and “also ran”-s) to turn their coats.